Involvement of Type I Hypersensitivity in Rapid Rejection of Trichinella spiralis from Adult Rats

Abstract

The role of type I hypersensitivity in the rapid rejection of Trichinella spiralis from actively, and passively immunized rats was examined. Net intestinal fluid secretion, which occurs during the rejection of the parasites, was used to verify the expression of local anaphylaxis and was examined for its possible role in the rejection process. Worm establishment in the small intestine 30 min after intraduodenal inoculation was significantly reduced in rats that were passively immunized with immune serum containing anti- Trichinella IgE as compared with recipients of normal serum. Worm-induced fluid secretion in immune rats was completely inhibited by the combined action of indomethacin and diphenhydramine. However, worm rejection was not affected. L-651,392, a 5-lipoxygenase inhibitor, also failed to prevent rejection. Ketanserin (a serotonin S₂ receptor antagonist) and MDL-72222 (a serotonin S₃ receptor antagonist) together blunted the rapid rejection response and reduced fluid secretion. Furthermore, intra-arterial perfusion of serotonin into nonimmune rats caused fluid secretion and reduced worm establishment. In nonimmune rats prostaglandin E₂, cholera toxin, and hypertonic Krebs-mannitol solution were used to evoke the same level of intestinal fluid secretion as that induced by reinfection in immune rats or by serotonin in nonimmune hosts. When larvae were inoculated into the secreting gut, their infectivity was unaffected. The results suggest that anaphylaxis is involved in the rapid rejection of T. spiralis in immune rats and that serotonin is a possible chemical mediator of worm rejection. Although the mode of action of serotonin in the rejection process remains unknown, its possible involvement through fluid secretion can be ruled out.

CYTOKINE REGULATION OF HOST DEFENSE AGAINST PARASITIC GASTROINTESTINAL NEMATODES:Lessons from Studies with Rodent Models*

“…In vitro studies have, in fact, demonstrated that exposure of the small intestine of T. spiralis-immune rats to T. spiralis antigen increases smooth muscle contractility, and that this response is dependent upon mast cell activation and 5-hydroxytryptamine, but not on histamine or prostaglandins (95). Consistent with this observation, the rapid rejection response is blunted in vivo when rats are treated with 5-hydroxytryptamine S2 and S3 receptor antagonists (ketanserin and MDL-72222, respectively), but not when they are treated with type 1 histamine (H1) receptor antagonists or with inhibitors of cyclooxygenase or 5-lipoxygenase (96).…”

Type I hypersensitivity reactions in intestinal mucosae from rats infected with Fasciola hepatica

“…There is a clear involvement of 'Type I' hypersensitivity reactions in mucosal defence against parasites which spend at least some of their life cycle in the gastro-intestinal tract (Moqbel & Pritchard 1990). Although immune rejection of an enteric parasite and antigen-evoked intestinal fluid secretion can be experimentally dissociated (Zhang & Castro 1990) it is not unlikely that a net secretion of fluid may complement other concomitant protective mechanisms. Ion transport responses were observed in small and large intestine from infected rats in keeping with previous findings that immunologic sensitization to parasites can influence different segments of the intestinal tract (Baird et al 1985).…”

T helper cell cytokine responses during intestinal nematode infection: induction, regulation and effector function.

“…Disruption of fluid secretion is also associated with rapid expulsion of challenge T. spiralis infection in rats (Castro et al, 1979). Furthermore, artificial increases in fluid secretion through administration of serotonin reduced the establishment of T. spiralis infection in naive rats (Zhang and Castro, 1990). Whether these responses are essential for expulsion of H. polygyrus and T. spiralis, or only contribute to the overall unfavourable environment for the worm in the intestine, is unclear at present.…”